Comparison of the cardiovascular effects of isoflurane and sevoflurane as measured by magnetic resonance imaging in children with congenital heart disease

STUDY OBJECTIVE: To compare the cardiovascular effects of isoflurane and sevoflurane at minimum alveolar concentration (MAC) = 1 in children with congenital heart disease using cardiac magnetic resonance imaging. DESIGN: Randomized, crossover, single-blinded study. SETTING: Tertiary-care teaching hospital. PATIENTS: 10 pediatric patients with congenital heart diseases scheduled to undergo cardiac magnetic resonance studies. INTERVENTIONS: Patients were randomized to receive either isoflurane or sevoflurane as the "first inhalation agent." After a period or more than 20 minutes, they were crossed over to receive the "second inhalation agent." MEASUREMENTS: Heart rate, mean arterial pressure (MAP), cardiac index, stroke volume index, and ejection fraction (EF) at one MAC for both agents were all recorded. MAIN RESULTS: Both isoflurane and sevoflurane caused a significant decrease in MAP from the baseline (P = 0.013). The mean values (+/-SD) of stroke volume (mL), cardiac index (L min(-1) m(-2)), and EF (%) for isoflurane versus sevoflurane were 21.5 (+/-9.2) versus 19.6 (+/-6.2), 4.1 (+/-1.2) versus 3.7 (+/-0.87), and 64.2 (+/-14.5) versus 62.5 (+/-13.8), respectively. CONCLUSION: Both isoflurane and sevoflurane were found to be comparable in terms of cardiovascular effects.     

Values of the bispectral index do not parallel the hemodynamic response to the rapid increase in isoflurane concentration

PURPOSE: To investigate the changes in hemodynamic variables and bispectral index (BIS) in response to a rapid increase in isoflurane or sevoflurane concentration. METHOD: Thirty adult patients were anesthetized with either isoflurane (isoflurane group) or sevoflurane (sevoflurane group). Two minutes after induction of anesthesia with thiamylal, the inspired concentrations of isoflurane and sevoflurane were rapidly increased from 0.5 minimum alveolar anaesthetic concentration (MAC) to 3 MAC and maintained for five minutes. Heart rate (HR), mean arterial pressure (MAP), and BIS were measured every minute. RESULTS: An increase in the anesthetic concentration caused increases in HR and MAP in the isoflurane group and a decrease in MAP in the sevoflurane group. Consequently, HR and MAP in the isoflurane group were significantly higher than those in the sevoflurane group. After inhalation of high concentrations, BIS significantly and progressively decreased in both groups. CONCLUSION: BIS values decrease after a step increase in volatile agent concentration, whether or not a hyperdynamic action occurs.     

Effects of halothane, isoflurane, and sevoflurane on lipid peroxidation following experimental closed head trauma in rats

Background: In a rat closed head trauma model we examined both the time course of lipid peroxidation and the effects of halothane, isoflurane, and sevoflurane on it by analysis of malondialdehyde (MDA) formation.
Methods: Animals were divided randomly into five groups: sham-operated (SO), n =18; control-closed head trauma to left frontal pole, n =18; closed head trauma model+halothane, n =18; closed head trauma model+isoflurane, n =18; and closed head trauma model+sevoflurane, n =18. Halothane, isoflurane, or sevoflurane were applied 15 min after trauma for 30 min. Rats were euthanized 1,3, and 5 h after the inhalation agents. Brain tissue samples were taken 5 mm from the left and right frontal poles. MDA was considered to reflect the degree of lipid peroxidation.
Results: MDA concentrations were greater in the control, halothane, sevoflurane, and isoflurane groups than in SO animals ( P <0.001). No statistical difference between the hemispheres was found between the halothane, isoflurane, or sevoflurane groups, but MDA levels were lower with isoflurane than in the halothane, sevoflurane, and control groups at 1, 3, and 5 h ( P <0.001). MDA levels were higher as compared with the halothane and sevoflurane groups at 1 h but not at 3 or 5 h ( P <0.001).
Conclusion: MDA levels with the isoflurane group were lower than in the other trauma groups, which suggest that isoflurane, given after closed head trauma, might be protective against lipid peroxidation of cerebral injury.     

Recovery and pharmacokinetic parameters of desflurane, sevoflurane, and isoflurane in patients undergoing urologic procedures.

STUDY OBJECTIVE: To compare the pharmacokinetics and the speed of recovery after inhalation anesthesia with desflurane, sevoflurane, and isoflurane in elective surgery. DESIGN: Prospective, randomized study. SETTING: University medical center. PATIENTS: 30 ASA physical status I and II adults presenting for elective surgery. INTERVENTIONS: Anesthesia was induced with etomidate and maintained with desflurane (n = 10), sevoflurane (n = 10), or isoflurane (n = 10) and nitrous oxide. The inhalation drugs were titrated until an adequate clinical depth of anesthesia was reached. At the end of anesthesia, the patients breathed oxygen via the endotracheal tube and after extubation via a face mask. MEASUREMENTS AND MAIN RESULTS: The groups were similar with respect to age, weight, duration of anesthesia, and mean arterial pressure. Mean end-tidal concentration (FA = FA0) at the end of anesthesia was 6.34 +/- 1.15% after desflurane, 1.85 +/- 0.42% after sevoflurane, and 1.10 +/- 0.24% after isoflurane. FA/FA0 decreased significantly faster with desflurane than with isoflurane, while there was little difference between desflurane and sevoflurane. As for the terminal half-life (t1/2), there were no differences among the groups (8.16 +/- 3.15 min after desflurane, 9.47 +/- 4.46 min after sevoflurane, and 10.0 +/- 5.57 min after isoflurane). The time until a command was followed for the first time was the same in all three groups (13.0 +/- 4.7 min after desflurane, 13.4 +/- 4.4 min after sevoflurane, and 13.6 +/- 3.4 min after isoflurane). There was no significant correlation between duration of anesthesia and the time until recovery. CONCLUSIONS: There are only minor differences with regard to the recovery phase in premedicated patients who receive clinically titrated inhalation anesthesia with desflurane, sevoflurane, or isoflurane.     

Sevoflurane and isoflurane, but not propofol, decrease mivacurium requirements over time

PURPOSE: Volatile anesthetic agents potentiate neuromuscular blockade, but the magnitude of potentiation appears to be time dependent. The time course of this interaction was studied by measuring mivacurium infusion rates during sevoflurane, isoflurane and propofol anesthesia. METHODS: After informed consent, anesthesia was induced in 48 ASA physical status I-II adults with propofol, fentanyl and mivacurium 0.25 mg.kg(-1) and maintained with N(2)O (60%) and one of the three agents chosen at random: sevoflurane 1.9%; isoflurane 1.2%; or propofol 100-150 microgram.kg(-1).min(-1). Train-of-four stimulation was applied every 15 sec to the ulnar nerve. Neuromuscular blockade was monitored with accelerometry. At 5% recovery of the first twitch (T1), a mivacurium infusion was started and adjusted every five minutes to maintain 90-95% T1 depression. RESULTS: The time to 5% T1 recovery after the initial dose was similar in all groups (13-15 min). Fifteen minutes after the start of the infusion mivacurium requirements were greater (P < 0.05) in the propofol group (7.5 +/- 1.7 microgram.kg(-1).min(-1); mean +/- SD) than in either isoflurane (4.7 +/- 1.6 microgram.kg(-1).min(-1)) or sevoflurane (4.5 +/- 1.5 microgram.kg(-1).min(-1)) group. Then, the rate remained stable for propofol (6.2 +/- 1.4 microgram.kg(-1).min(-1) after 90 min of infusion) while it decreased with isoflurane to 2.9 +/- 1.6 microgram.kg(-1).min(-1) at 90 min (P < 0.05 vs propofol) and to 1.4 +/- 1.0 microgram.kg(-1).min(-1) in the sevoflurane group (P < 0.05 vs propofol and isoflurane). CONCLUSION: Sevoflurane and isoflurane do not prolong the effect of a bolus dose of mivacurium, but potentiation increases with time from 30-105 min of exposure. This interaction is greater with sevoflurane than isoflurane.     

七氟醚与异氟醚苏醒期熵指数和听觉诱发电位指数的相关性

目的观察七氟醚和异氟醚苏醒期熵指数(RE和SE)与听觉诱发电位指数(AAI)的变化和相关性。方法择期行腹腔镜下胆囊或子宫附件切除术患者30例,随机均分为七氟醚组(S组)和异氟醚组(I组),分别持续吸入2%～3%七氟醚和异氟醚维持麻醉。吸入麻醉药停止后,20min内每隔1分钟记录RE、SE与AAI,并分析其相关性。结果苏醒期RE、SE与AAI均呈逐渐上升趋势,Ⅰ组相关系数分别为0.89和0.91(P<0.05);S组相关系数分别为0.93和0.91(P<0.05)。结论熵指数和AAI均能反映七氟醚和异氟醚苏醒期麻醉深度的变化,两者相关性良好。     

异氟醚、七氟醚吸入麻醉对鼠骨骼肌微循环白细胞活动的影响

目的 探讨异氟醚、七氟醚吸入麻醉对鼠骨骼肌微循环白细胞活动的影响。方法 选择SD雄性大鼠20只,随机分为两组,制备提睾肌微循环模型。吸入异氟醚、七氟醚麻醉后,分别记录吸入异氟醚、七氟醚1．5MAC3h内微循环、小动脉A1的直径和血流速度,微循环毛细血管后微静脉的白细胞滚动和粘附数量。结果 吸入异氟醚、七氟醚1．5MAC3h内HR,MAP,CVP和A1的直径和血流速度无明显改变（P＞0．05）。微循环毛细血管后微静脉的白细胞流动和粘附数量显著增加（P＜0．01）。结论 长时间吸入异氟醚、七氟醚后,可引起大鼠骨骼肌微循环毛细血管后微静脉的白细胞滚动和粘附数量显著增加。     

The effects of volatile anesthetics on nonadrenergic,noncholinergic depressor responses in rats

The effects of volatile anesthetics on nonadrenergic, noncholinergic (NANC) transmission mediated by calcitonin gene-related peptide (CGRP) are unclear. We studied the effects of isoflurane, halothane, and sevoflurane on NANC depressor responses to electrical spinal cord stimulation in pithed rats whose mean arterial blood pressure was maintained near 120 mm Hg by continuous infusion of methoxamine. Autonomic outflow was blocked by hexamethonium. After 30 min of inhalation of different concentrations of anesthetics, spinal cord stimulation at the lower thoracic level (10 V at 4 Hz; duration, 1 ms) was applied for 30 s to induce a NANC depressor response. Isoflurane at 2% and halothane at 1.5% attenuated NANC depressor responses significantly, whereas isoflurane at 1%, halothane at 0.75%, and sevoflurane at 2% or 4% did not. Volatile anesthetics did not attenuate the release of CGRP after spinal cord stimulation, whereas isoflurane at 2% and halothane at 1.5% significantly inhibited depressor responses to exogenously administered CGRP. Sevoflurane at 4% did not significantly affect CGRP-induced depressor responses. Thus, isoflurane and halothane at large concentrations attenuate NANC depressor responses by attenuating the depressor action of CGRP, not CGRP release. IMPLICATIONS: The anesthetics isoflurane and halothane attenuate nonadrenergic, noncholinergic depressor responses mediated by calcitonin gene-related peptide in the rat without affecting the release of the peptide.     

Effects of enflurane, isoflurane, sevoflurane and desflurane on reperfusion injury after regional myocardial ischaemia in the rabbit heart in vivo

It is known that volatile anaesthetics protect myocardial tissue against ischaemic and reperfusion injury in vitro. In this investigation, we have determined the effects of the inhalation anaesthetics, enflurane, isoflurane, sevoflurane and desflurane, administered only during early reperfusion, on myocardial reperfusion injury in vivo. Fifty chloralose-anaesthetized rabbits were subjected to 30 min of occlusion of a major coronary artery followed by 120 min of reperfusion. Left ventricular pressure (LVP, tip-manometer), cardiac output (CO, ultrasonic flow probe) and infarct size (triphenyltetrazolium staining) were determined. During the first 15 min of reperfusion, five groups of 10 rabbits each received 1 MAC of enflurane (enflurane group), isoflurane (isoflurane group), sevoflurane (sevoflurane group) or desflurane (desflurane group), and 10 rabbits served as untreated controls (control group). Haemodynamic baseline values were similar between groups (mean LVP 106 (SEM 2) mm Hg; CO 281(7) ml min-1). During coronary occlusion, LVP and CO were reduced to the same extent in all groups (LVP 89% of baseline; CO 89%). Administration of inhalation anaesthetics during early reperfusion further reduced both variables, but they recovered after discontinuation of the anaesthetics to values not different from control animals. Infarct size was reduced from 49 (5)% of the area at risk in the control group to 32 (3)% in the desflurane group (P = 0.021), and to 36 (2)% in the sevoflurane group (P = 0.097). In the enflurane group, infarct size was 39 (5)% (P = 0.272). Isoflurane had no effect on infarct size (48 (5)%, P = 1.000). The results show that desflurane and sevoflurane markedly reduced infarct size and therefore can protect myocardium against reperfusion injury in vivo. Enflurane had only a marginal effect and isoflurane offered no protection against reperfusion injury in vivo. These different effects suggest different protective mechanisms at the cellular level.      

Isoflurane and sevoflurane during reperfusion prevent recovery from ischaemia in mitochondrial KATP channel blocker pretreated hearts

BACKGROUND AND OBJECTIVE: Inhalation anaesthetics given only during post-ischaemic reperfusion have some protective effect against reperfusion injury in the heart. Adenosine triphosphate-regulated mitochondrial potassium channels have been shown to be an important mediator of cardioprotection. Thus, we investigated whether 5-hydroxydecanoate, a putative mitochondrial potassium channel blocker, prevents the cardioprotective effect of volatile anaesthetics. METHODS: Forty rats were randomly allocated to four groups of equal size: control group, 5-hydroxydecanoate group, 5-hydroxydecanoate + sevoflurane group and 5-hydroxydecanoate + isoflurane group. Seven minutes after the start of perfusion, normal saline (control group) or 5-hydroxydecanoate (the other groups) was administered. Ten minutes after the start of perfusion, the heart was rendered globally ischaemic for 10 min. One minute before the end of the ischaemic period, 2.7% sevoflurane or 1.4% isoflurane were administered in the 5-hydroxydecanoate + sevoflurane or 5-hydroxydecanoate + isoflurane groups respectively. The heart was reperfused for 10 min. RESULTS: Adenosine triphosphate content at the end of reperfusion in the 5-hydroxydecanoate + sevoflurane group was significantly lower (P < 0.05) than those in the control and the 5-hydroxydecanoate + isoflurane groups (19.9 +/- 8.7, 28.1 +/- 3.4 and 30.4 +/- 2.3 micromol g(-1), respectively). In addition, the combination of inhalation anaesthetics and 5-hydroxydecanoate decreased the ratios of recovered hearts from ischaemia (5-hydroxydecanoate + sevoflurane group: 40%, 5-hydroxydecanoate + isoflurane group 50%). CONCLUSION: 5-hydroxydecanoate alone caused no significant changes in haemodynamics and myocardial metabolism. However, the combination of 5-hydroxydecanoate and volatile anaesthetics impaired the recovery from ischaemia. Although animal data cannot be extrapolated to human beings, we suggest that more attention be paid to patients on sulphonylurea drugs, which inhibit potassium channels, when they are anaesthetized with volatile anaesthetics.     

Pulmonary mechanics during isoflurane,sevoflurane and desflurane anaesthesia

This study was designed to investigate the effects of desflurane on bronchial smooth muscle tone, following intubation and to compare these effects with isoflurane and sevoflurane. Patients were randomly divided into three groups to receive, isoflurane (n = 22), sevoflurane (n = 23), or desflurane (n = 22). Peak inspiratory pressure (PIP), respiratory resistance (Rr) and dynamic compliance (Cdyn) measurements were recorded at three time points; After the beginning of ventilation and before inhalation agent was started, following 5 min of ventilation with 1 MAC (minimum alveolar concentration) inhalation agent and following 5 min of 2 MAC inhalation agent. We found that all inhalation agents caused a significant decrease in Peak Inspiratory Pressure (PIP) and respiratory resistance (Rr), and an increase in dynamic compliance (Cdyn) at 1 MAC concentrations. When the agent concentration was increased to 2 MAC, desflurane caused a significant increase in Rr and PIP and a decrease in Cdyn. We concluded that desflurane, like isoflurane and sevoflurane, exhibits a bronchodilator effect at 1 MAC concentration. However, increasing the concentration to 2 MAC caused an increase in airway resistance with desflurane, whilst sevoflurane and isoflurane continued to have a bronchodilator effect.     

Rocuronium potency and recovery characteristics during steady-state desflurane, sevoflurane, isoflurane or propofol anaesthesia

We have studied the potency and recovery characteristics of rocuronium during 1.25 MAC of isoflurane, desflurane, sevoflurane or propofol anaesthesia in 84 patients using electromyography. Potency was determined by a cumulative bolus technique. The mean ED50 of rocuronium was 169 (SD 41), 126 (32), 121 (28) and 136 (25) micrograms kg-1 during propofol, isoflurane, sevoflurane and desflurane anaesthesia, respectively (ns), and ED90 values were 358 (62), 288 (29), 289 (28) and 250 (28) micrograms kg-1, respectively. The reduction in ED90 was statistically significant for all three inhalation anaesthetics (P < 0.05) compared with propofol. After 120 min, the cumulative infusion rate of rocuronium to obtain twitch depression of 90-95% was 9.0 (1.9), 6.3 (1.6), 6.1 (2.0) and 6.1 (1.1) micrograms kg-1 min-1 during propofol, isoflurane, sevoflurane and desflurane anaesthesia, respectively (P < 0.01). Recovery index was 22 (13), 27 (10), 28 (13) and 26 (14) min under propofol, isoflurane, sevoflurane and desflurane anaesthesia, respectively (ns). There were no significant differences between the three potent inhalation anaesthetics in relation to potency, infusion requirements or recovery characteristics of rocuronium.      

Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane on myocardial reperfusion injury in the isolated rat heart

A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation anaesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts perfused at a constant flow (10 ml min-1, PO2 80 kPa) and paced at 350 beat min-1, we determined left ventricular developed pressure (LVDP) and release of creatine kinase (CKR) as indices of myocardial performance and cellular injury, respectively. Seven control hearts underwent 30 min of no-flow ischaemia and 1 h of reperfusion. In the treatment groups, halothane, enflurane, isoflurane, sevoflurane or desflurane (each group n = 6) was added to the perfusion medium for the first 30 min of reperfusion at a concentration corresponding to 1.5 MAC in the rat. In the control group, cellular injury occurred at early reperfusion (peak CKR 283 (SEM 57) iu litre-1 at 10 min of reperfusion). Peak CKR to the coronary venous effluent was attenuated by all anaesthetics (halothane group 156 (45), enflurane group 134 (20), sevoflurane group 132 (20), desflurane group 159 (25) iu litre-1; each P < 0.05). Isoflurane did not differ from controls (303 (53) iu litre-1; P = 0.5). In the sevoflurane group, there was a delayed peak CKR after discontinuation of the anaesthetic at 30 min of reperfusion (260 (34) iu litre-1). Functional recovery was improved by all anaesthetics, but was seen much earlier with desflurane (LVDP 28 (3)% of baseline at 5 min reperfusion compared with halothane (6 (1)%), enflurane (11 (3)%), isoflurane (9 (6)%), sevoflurane (10 (2)%) and controls (3 (1)% of baseline)). At 30 min of reperfusion, recovery of LVDP was improved to a similar extent by all anaesthetics (halothane 30 (9)%, enflurane 36 (9)%, isoflurane 33 (5)%, sevoflurane 30 (5)%, desflurane 36 (4)% of baseline values) compared with controls (13 (5)%; each P < 0.05). All inhalation anaesthetics protected against myocardial reperfusion injury, but showed differences in attenuation of cellular injury and functional recovery. These differences may suggest different protective mechanisms.      

Effects of isoflurane, sevoflurane, and halothane on myofilament Ca2+ sensitivity and sarcoplasmic reticulum Ca2+ release in rat ventricular myocytes

BACKGROUND: The aim of this study was to describe and compare the effects of isoflurane, sevoflurane, and halothane at selected concentrations (i.e., concentrations that led to equivalent depression of the electrically evoked Ca2+ transient) on myofilament Ca2+ sensitivity, sarcoplasmic reticulum (SR) Ca2+ content, and the fraction of SR Ca2+ released during electrical stimulation (fractional release) in rat ventricular myocytes. METHODS: Single rat ventricular myocytes loaded with fura-2 were electrically stimulated at 1 Hz, and the Ca2+ transients and contractions were recorded optically. Cells were exposed to each anesthetic for 1 min. Changes in myofilament Ca2+ sensitivity were assessed by comparing the changes in the Ca2+ transient and contraction during exposure to anesthetic and low Ca2+. SR Ca2+ content was assessed by exposure to 20 mm caffeine. RESULTS: Isoflurane and halothane caused a depression of myofilament Ca2+ sensitivity, unlike sevoflurane, which had no effect on myofilament Ca2+ sensitivity. All three anesthetics decreased the electrically stimulated Ca2+ transient. SR Ca2+ content was reduced by both isoflurane and halothane but was unchanged by sevoflurane. Fractional release was reduced by both isoflurane and sevoflurane, but was unchanged by halothane. CONCLUSIONS: Depressed myofilament Ca2+ sensitivity contributes to the negative inotropic effects of isoflurane and halothane but not sevoflurane. The decrease in the Ca2+ transient is either responsible for or contributory to the negative inotropic effects of all three anesthetics and is either primarily the result of a decrease in fractional release (isoflurane and sevoflurane) or primarily the result of a decrease in SR Ca2+ content (halothane).     

Cardioprotection against reperfusion injury is maximal with only two minutes of sevoflurane administration in rats

PURPOSE: Volatile anesthetics can protect the heart against reperfusion injury. When sevoflurane is given for the first 15 min of reperfusion, a concentration corresponding to one minimum alveolar concentration (MAC) provides a maximum protective effect. The present study addresses the question of how long sevoflurane has to be administered to achieve the best cardioprotection. METHODS: Chloralose anesthetized rats were subjected to a 25-min occlusion of a major coronary artery, followed by 90 min of reperfusion. During the initial phase of reperfusion, an end-tidal concentration of 2.4 vol.% of sevoflurane (1 MAC) was given for two (n = 8), five (n = 8) or ten minutes (n = 7). Seven rats served as untreated controls. We measured left ventricular (LV) pressure, mean aortic pressure and infarct size (triphenyltetrazolium staining). RESULTS: Administration of sevoflurane for two minutes resulted in the greatest reduction of infarct size to 15% (8-22 [mean (95% confidence interval)] of the area at risk compared with controls [51 (47-55) %, P < 0.001]. Five or ten minutes of sevoflurane administration reduced infarct size to 26 (18-34) and 26 (18-35) % [P < 0.05], respectively. The cardiodepressant effect of sevoflurane varied with the duration of its administration: LV dP/dt was reduced from 6332 mmHg x sec(-1) (5771-6894) during baseline to 4211 mmHg x sec(-1) (3031-5391), 3811 mmHg x sec(-1) (2081-5540) and 3612 mmHg x sec(-1) (2864-4359) after two, five and ten minutes of reperfusion, respectively. CONCLUSION: Administration of 1 MAC sevoflurane for the first two minutes of reperfusion effectively protects the heart against reperfusion injury in rats in vivo. A longer administration time had lesser cardioprotective effects in this experimental model.     

Emergence agitation in preschool children: double-blind, randomized, controlled trial comparing sevoflurane and isoflurane anesthesia

BACKGROUND: This randomized, double-blind controlled trial was conducted to determine whether the association of sevoflurane for induction and isoflurane for anesthesia maintenance resulted in a lower incidence of postoperative agitation compared with sevoflurane as single agent. METHODS: After Institute Ethics Committee's approval and parental written informed consent, 128 unpremedicated children (1-6 years), ASA I-II, scheduled for elective subumbilical surgery were enrolled. After induction with 8% sevoflurane, patients were randomly allocated to receive sevoflurane or isoflurane 1-1.5 MAC as maintenance agent. The primary endpoint of the study was the incidence of postoperative agitation defined as a screaming and crying child and/or a child that required physical restraint during emergence. RESULTS: Eighteen children were excluded because they received sedatives, analgesia or anesthesia or because of ineffective regional analgesia before randomization. Fifty-four patients receiving sevoflurane and 56 receiving isoflurane completed the study. Twenty-eight children (95% CI 38-66%) in the sevoflurane group presented with postoperative agitation compared with 18 (95% CI 20-46%) patients receiving isoflurane (P = 0.028). Fifteen minutes after awakening, 11/54 children receiving sevoflurane were agitated compared with 4/56 receiving isoflurane (P = 0.03). Thereafter, there was a gradual reduction in the incidence of postoperative agitation over time. CONCLUSIONS: The association of sevoflurane for induction and isoflurane for maintenance produced significant less postoperative agitation in preschool children receiving regional anesthesia during subumbilical surgery compared with sevoflurane for induction and maintenance.     

七氟醚预处理联合后处理对大鼠心肌缺血再灌注时血栓素A2和前列腺素I2的影响

目的 评价七氟醚预处理联合后处理对大鼠心肌缺血再灌注时血栓素A2和前列腺素I2的影响.方法 健康雄性Wistar大鼠50只,体重250～280 g,采用随机数字表法,将大鼠随机分为5组(n=10):假手术组(S组)、缺血再灌注组(I/R组)、七氟醚预处理组(Spr组)、七氟醚后处理组(Spo组)和七氟醚预处理联合七氟醚后处理组(Spr+po组).I/R组、Spr组、Spo组和Spr+po组采用结扎左冠状动脉前降支30 min时进行再灌注的方法制备心肌缺血再灌注模型,S组仅在左冠状动脉前降支下穿线.Spr组进行七氟醚预处理:于缺血前30 min吸入2.5%七氟醚15 min,洗脱15 min;Spo组进行七氟醚后处理:再灌注前1 min开始吸入2.5%七氟醚,持续5 min;Spr+po组进行七氟醚预处理和后处理.再灌注2 h时取动脉血样,测定血MB型磷酸肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、心肌肌钙蛋白I(cTnI)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)的水平和血小板最大聚集率,并计算TXB2与6-keto-PGF1α的比值(TXB2/6-keto-PGF1α).取心肌组织,电镜下观察病理学结果,进行线粒体损伤评分,并测定线粒体的比表面和面数密度.结果 与S组比较,I/R组血CK-MB、LDH、cTnI、TXB2、6-keto-PGF1α的水平、TXB2/6-keto-PGF1α血小板最大聚集率及线粒体损伤评分升高,线粒体的比表面和面数密度降低(P<0.05或0.01);与I/R组比较,Spr组和Spo组血CK-MB、LDH、cTnI的水平、TXB2/6-keto-PGF1α和线粒体损伤评分降低,血6-keto-PGF1α浓度、线粒体的比表面和面数密度升高(P<0.05或0.01);与Spr组和Spo组比较,Spr+po组血CK-MB、LDH、cTnI、TXB2的水平、TXB2/6-keto-PGF1α血小板最大聚集率和线粒体损伤评分降低,血6-keto-PGF1α浓度、线粒体的比表面和面数密度升高(P<0.05).Spr+po组心肌损伤程度轻于Spr组和Spo组.结论 与七氟醚预处理或后处理比较,两种方法联合应用可抑制血栓素A2的释放和促进前列腺素I2的释放,从而进一步减轻了大鼠心肌缺血再灌注损伤.

Abstract：

Objective To investigate the effect of sevoflurane preconditioning-postconditioning on thromboxane A2 and prostaglandin I2 during myocardial ischemia-reperfusion (I/R) in rats. Methods Fifty healthy male Wistar rats weighing 250-280 g were randomly divided into 5 groups (n = 10 each) : sham operation group (group S) , I/R group, sevoflurane preconditioning group (group Spr), sevoflurane postconditioning group (group Spo)and combination of sevoflurane preconditioning and postconditioning group (group Spr + po). Myocardial I/R was produced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h reperfusion in anesthetized rats. In group S the anterior descending branch was only exposed but not ligated. Group Spr received 15 min inhalation of 2.5 % sevoflurane and 15 min wash-out 30 min before ischemia. Group Spo received 5 min inhalation of 2.5% sevoflurane 1 min before reperfusion. Arterial blood samples were taken at 2 h of reperfusion for determination of the levels of MB isoenzyme of creatine kinase (CK-MB) , lactate dehydrogenase (LDH) , cardiac troponin I (cTnI), thromboxane B2(TXB2), and 6-keto-prostaglandin (6-keto-PGF1α) and platelet maximum aggregation rate. TXB2/6-keto-PGF1α ratio was calculated. The myocardial tissues were taken for microscopic examination. Mitochondria] injury was assessed by using Flameng score and stereology (Specific surface, δ and Numerical density on area, NA) .Results Compared with group S, the levels of CK-MB, LDH, cTnI, TXE2 and 6-ketoPGF1α, TXB2/6-keto-PGF1α ratio, platelet maximum aggregation rate and Flameng score were significantly increased, while δ and NA were significantly decreased in group I/R (P < 0.05 or 0.01) . The levels of CK-MB,LDH and cTnI, TXB2/6-keto-PGF1α ratio and Flameng score were significantly lower, and 6-keto-PGF1α level, δand NA were significantly higher in Spr and Spo groups than in group I/R ( P < 0.05 or 0.01) . The levels of CKMB, LDH, cTnI and TXB2 , TXB2/6-keto-PGF1α ratio, platelet maximum aggregation rate and Flameng score were significantly lower and 6-keto-PGF1α level,δ and NA were significantly higher in group Spr + po than in Spr and Spo groups(P < 0.05). Conclusion Sevoflurane preconditioning-postconditioning can reduce myocardial I/R injury through inhibiting the release of thromboxane A2 and promoting the release of prostaglandin I2 in rats.     

Comparison of recovery after intermediate duration of anaesthesia with sevoflurane and isoflurane

BACKGROUND: The purpose of this study was to compare recovery from anaesthesia after sevoflurane and isoflurane were administered to children for more than 90 min. METHODS: After parental informed consent and ethical committee approval, children aged between 2 months and 6 years, ASA I or II, were randomly allocated to sevoflurane (n=20) or isoflurane (n=20) groups. Halogenated agents were discontinued following skin closure and patients were ventilated mechanically with 100% oxygen until minimum alveolar concentration (MAC) values awake were obtained (endtidal concentrations 0.6 MAC for sevoflurane and 0.4 MAC for isoflurane). Effective perioperative analgesia was provided by a caudal block. RESULTS: The mean (+/- SD) duration of anaesthesia was 132 +/- 38 min and 139 +/- 49 min for sevoflurane and isoflurane, respectively. Early recovery occurred sooner in the isoflurane group (time to extubation was 16 +/- 7 min and 11 +/- 5 min, P<0.01; Aldrete's score at 0 min was 5.5 +/- 1.5 and 7.4 +/- 1.8, P<0.001, respectively). But the time to be fit for discharge from recovery room was similar at 136 +/- 18 min and 140 +/- 20 min, respectively. CONCLUSIONS: After intermediate duration of anaesthesia administered to children for up to 90 min, isoflurane and sevoflurane allow recovery after approximatively the same lapse of time.     

The effects of sevoflurane and isoflurane on intracranial pressure and cerebral perfusion pressure after diffuse brain injury in rats

Twenty-four adult male Wistar rats, weighing 220 to 290 g, were anesthetized with 30 mg/kg intraperitoneal sodium thiopental, then underwent a tracheostomy. After diffuse impact-acceleration brain injury (BI) was induced, each rat was paralyzed and mechanically ventilated with 30% O2 in nitrous oxide (N2O). The rats were assigned randomly to two groups, each of which received one of the two volatile anesthetic agents, sevoflurane or isoflurane. The anesthetics were administered at 0.5, 0.75, 1.0, and 1.25 minimal alveolar concentration (MAC) for 30 minutes each, respectively, and anesthesia was maintained at 0.75 MAC during the last hour of the study period. Intracranial pressure (ICP), mean arterial pressure (MAP), rectal and intrahemispheric temperatures, and end-tidal volatile anesthetic concentrations were monitored continuously throughout the 3 hours, with measurements recorded every 15 minutes. At baseline, there were no significant differences between the two groups regarding the monitored physiologic values. In the sevoflurane group, MAP fell significantly after 45 minutes, and a similar change was observed in the isoflurane group after 30 minutes (P < .05, P < .01, and P < .001, respectively). Intracranial pressure increased significantly at 45 minutes in the sevoflurane group (P < .01) and remained elevated from 60 minutes until the end of the study period (P < .01, P < .001). Although ICP increased in the isoflurane group, the change was not significant. Cerebral perfusion pressure (CPP) decreased in parallel with MAP, with the reduction in the sevoflurane group being more pronounced than that in the isoflurane group. The results demonstrated that, under the conditions of diffuse BI, animals that were anesthetized with sevoflurane had higher ICP and lower CPP levels than those anesthetized with isoflurane.     

Clinical comparison of sevoflurane and isoflurane when administered with nitrous oxide for surgical procedures of intermediate duration

The purpose of this study was to compare the haemodynamic effects and emergence times of anaesthesia with sevoflurane with those of isoflurane when the agents were administered with nitrous oxide to adult inpatients (ASA I and II) undergoing surgery of at least an hour in duration. Fifty patients were randomly assigned to receive either 0.65 minimum alveolar concentration (MAC) (1.3%) sevoflurane or 0.65 MAC (0.8%) isoflurane together with 60% nitrous oxide following induction with thiopentone, fentanyl, and succinylcholine. Systemic blood pressure and heart rate trends were similar for both groups for the duration of anaesthesia. However, differences in systolic blood pressure measurements were noted at one minute after incision (99 ± 3 mmHg, mean ± SE, in the sevoflurane group compared with 109 ± 4 mmHg for isoflurane), and at emergence (125 ± 3 mmHg for sevoflurane, 134 ± 3 mmHg for isoflurane), and in diastolic blood pressure measurements at five minutes after intubation (64 ± 2 mmHg for sevoflurane, 73 ± 3 mmHg for isoflurane). Recovery of response to command was more rapid after discontinuation of sevofluranenitrous oxide (9.9 ± 1.1 min) than after isoflurane-nitrous oxide (13.9 ± 1.3 min). Despite earlier emergence, patients who had received sevoflurane did not request postoperative analgesia sooner. We conclude that the purported advantages of sevoflurane, namely haemodynamic stability and rapid emergence, can be expected even when the agent is administered at 0.65 MAC (1.3%) in nitrous oxide to a typical adult surgical population undergoing procedures of intermediate duration (2.3 ± 0.2 hr).